Peruru Rupasree, Usha Rani R, Thatiparthi Jhansyrani, Sampathi Sunitha, Dodoala Sujatha, Prasad K V S R G
Institute of Pharmaceutical Technology, Sri Padmavati Mahila Visvavidyalayam, Tirupati, India.
National Institute of Pharmaceutical Education and Research-Hyderabad, India.
Heliyon. 2020 May 8;6(5):e03921. doi: 10.1016/j.heliyon.2020.e03921. eCollection 2020 May.
Over 200 million people are exposed to arsenic worldwide in their daily lives. Arsenic is a toxic ubiquitous metalloid distributed in the ground water. From the last few decades it is obtaining considerable attention for its severe neurotoxic properties. In this study the neuroprotective efficacy of devil's claw (DCW), a potent antioxidant has been investigated against arsenic induced neurotoxicity in female rats. Neurotoxicity was established by oral administration of 13 mg/kg sodium arsenite. The animals were divided into five groups (n = 6) including normal control, disease/arsenic control, standard treatment (Apocynin, 10 mg/kg), DCW treatment I (DCW, 200 mg/kg) and DCW treatment II (DCW, 400 mg/kg). Exploratory, anxiety and motor coordination related behavior of the animals was assessed using hole-board, forced swimming, beam walk and elevated plus maze tests. Findings revealed that DCW treatment ameliorated anxiety and motor in-coordination in the rats compared to the arsenic control group. In addition, arsenic induced a significant oxidative stress in arsenic only treated group, whereas co-administration with DCW the oxidative stress was reduced prominently. Arsenic control group produced gliosis and nuclear pyknosis of the brain cells which were prominently suppressed with the treatment of DCW for 21 days. The activity of DCW was in correlation with the concentration of harpagoside in the serum estimated by the HPLC method, supports that harpagoside was the active constituent responsible for neuroprotective effect. Further findings are required to understand the molecular mechanisms involved in neuroprotective effect of harpagoside and DCW.
全球有超过2亿人在日常生活中接触到砷。砷是一种有毒且广泛存在的类金属,分布于地下水中。在过去几十年里,因其严重的神经毒性特性,它受到了相当大的关注。在本研究中,已对一种强效抗氧化剂魔鬼爪(DCW)对雌性大鼠砷诱导的神经毒性的神经保护作用进行了研究。通过口服13 mg/kg亚砷酸钠建立神经毒性。将动物分为五组(n = 6),包括正常对照组、疾病/砷对照组、标准治疗组(Apocynin,10 mg/kg)、DCW治疗组I(DCW,200 mg/kg)和DCW治疗组II(DCW,400 mg/kg)。使用洞板试验、强迫游泳试验、横梁行走试验和高架十字迷宫试验评估动物的探索性、焦虑和运动协调相关行为。研究结果表明,与砷对照组相比,DCW治疗改善了大鼠的焦虑和运动不协调。此外,砷在仅接受砷治疗的组中诱导了显著的氧化应激,而与DCW共同给药时,氧化应激显著降低。砷对照组出现了脑细胞胶质增生和核固缩,而用DCW治疗21天可显著抑制这些现象。DCW的活性与通过高效液相色谱法测定的血清中哈帕苷浓度相关,这支持哈帕苷是具有神经保护作用的活性成分。需要进一步的研究来了解哈帕苷和DCW神经保护作用所涉及的分子机制。